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Sant Antoni de Portmany, Spain

Alijotas-Reig J.,systemIC | Alijotas-Reig J.,Vall Dhebron University Hospital | Alijotas-Reig J.,Autonomous University of Madrid | Garcia-Gimenez V.,Europa Medical Center | And 4 more authors.
Lupus | Year: 2012

Background: Systemic autoimmune/granulomatous adverse reactions related to biomaterials other than silicone have rarely been reported. Aim: The aim of this paper is to communicate the cases of autoimmune/inflammatory syndrome induced by adjuvants (ASIA) in a study of Spanish patients suffering from inflammatory disorders related to biomaterial injections other than silicone, principally hyaluronic acid, acrylamides or methacrylate compounds. Methods: The authors performed a retrospective analysis of the clinical, laboratory, histopathology and follow-up of a cohort of 250 cases of patients suffering from inflammatory/autoimmune disorders related to bioimplant injections. Results: Of these 250 cases, patients with adverse reactions related to silicone injections (n=65) were excluded. Of the remaining 185, 15 cases (8%) had systemic or distant and multiple complaints that could be categorized as ASIA. In all but four patients, inflammatory features at the implantation site preceded distant or systemic manifestations. Abnormal blood tests were common. Eleven cases (73.3%) with inflammatory localized nodules and panniculitis evolved into a variety of disorders, namely, primary biliary cirrhosis, Sjögren's syndrome, sarcoidosis, human adjuvant disease and inflammatory polyradiculopathy. Four cases presented primarily with systemic autoimmune disorders. Conclusions: Infrequently, biomaterials other than silicone can provoke local inflammatory adverse reactions that may evolve into systemic autoimmune and/or granulomatous disorders. Whether or not these biomaterials act as an adjuvant, they could be included in the ASIA category. © The Author(s), 2012. Reprints and permissions: http://www.sagepub.co.uk/ journalsPermissions.nav.


Juanola-Falgarona M.,Rovira i Virgili University | Juanola-Falgarona M.,Institute Salut Carlos III | Salas-Salvado J.,Rovira i Virgili University | Salas-Salvado J.,Institute Salut Carlos III | And 13 more authors.
American Journal of Clinical Nutrition | Year: 2014

Background: Low-glycemic index (GI) diets have been proven to have beneficial effects in such chronic conditions as type 2 diabetes, ischemic heart disease, and some types of cancer, but the effect of low-GI diets on weight loss, satiety, and inflammation is still controversial. Objective: We assessed the efficacy of 2 moderate-carbohydrate diets and a low-fat diet with different GIs on weight loss and the modulation of satiety, inflammation, and other metabolic risk markers. Design: The GLYNDIET study is a 6-mo randomized, parallel, controlled clinical trial conducted in 122 overweight and obese adults. Participants were randomly assigned to one of the following 3 isocaloric energy-restricted diets for 6 mo: 1) a moderate-carbohydrate and high-GI diet (HGI), 2) a moderate-carbohydrate and low-GI diet (LGI), and 3) a low-fat and high-GI diet (LF). Results: At weeks 16 and 20 and the end of the intervention, changes in body mass index (BMI; in kg/m2) differed significantly between intervention groups. Reductions in BMI were greater in the LGI group than in the LF group, whereas in the HGI group, reductions in BMI did not differ significantly from those in the other 2 groups (LGI: 22.45 ± 0.27; HGI: 22.30 ± 0.27; LF: 21.43 ± 0.27; F = 4.616, P = 0.012; pairwise comparisons: LGI compared with HGI, P = 1.000; LGI compared with LF, P = 0.016; HGI compared with LF, P = 0.061). The decrease in fasting insulin, homeostatic model assessment of insulin resistance, and homeostatic model assessment of β cell function was also significantly greater in the LGI group than in the LF group (P <0.05). Despite this tendency for a greater improvement with a low-GI diet, the 3 intervention groups were not observed to have different effects on hunger, satiety, lipid profiles, or other inflammatory and metabolic risk markers. Conclusion: A low-GI and energy-restricted diet containing moderate amounts of carbohydrates may be more effective than a high-GI and low-fat diet at reducing body weight and controlling glucose and insulin metabolism. This trial was registered at Current Controlled Trials (www.controlled-trials.com) as ISRCTN54971867. © 2014 American Society for Nutrition.


Garcia-Vidal C.,Hospital Universitari Of Bellvitge | Garcia-Vidal C.,Institute Salut Carlos III | Barba P.,Hospital Universitari Vall dHebron | Arnan M.,Hospital Duran I Reynals | And 10 more authors.
Clinical Infectious Diseases | Year: 2011

We report 5 cases of invasive aspergillosis occurring in severely immunosuppressed patients hospitalized with pandemic influenza A (H1N1). We suggest that infection with influenza A (H1N1) may predispose immunocompromised patients to develop invasive aspergillosis. Physicians should be aware of this potential association to allow early diagnosis and prompt treatment of aspergillosis. © 2011 The Author.


Arderiu G.,Institute Salut Carlos III | Pena E.,Institute Salut Carlos III | Aledo R.,Institute Salut Carlos III | Espinosa S.,Institute Salut Carlos III | Badimon L.,Institute Salut Carlos III
Angiogenesis | Year: 2012

Tissue factor (TF) has well-recognized roles as initiator of blood coagulation as well as an intracellular signaling receptor. TF signaling regulates gene transcription and protein translation. Recently, we have shown that TFinduced mature neovessel formation is ultimately driven by CCL2 expression. However, the signaling process induced by TF to promote microvessel formation remains to be determined. This study was designed with the objective to investigate the mechanisms involved in TF-induced neovessel formation. Here, we have identified that Ets-1 expression is a downstream effector of TF signaling. TFsiRNA induced a highly significant reduction in Ets-1 expression levels and in Ets-1/DNA binding while inducing abrogation of microvessel formation. Activation of Ets-1 rescued the effect of TF inhibition and restored microvessel formation confirming the critical role of Ets-1 in TF-induced angiogenesis. VE-cadherin expression, a key regulator of endothelial intercellular junctions, and an Ets-1 target molecule was dependent of TF-inhibition. We show that TF signals through ERK1/2 to activate Ets-1 and induce CCL2 gene expression by binding to its promoter region. We conclude that endothelial cell TF signals through ERK1/2 and Ets-1 to trigger microvessel formation. © Springer Science+Business Media B.V. 2012.

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